Infiltrating myeloid cell-derived properdin markedly promotes microglia-mediated neuroinflammation after ischemic stroke.

BACKGROUND: Emerging evidence has shown that myeloid cells that infiltrate into the peri-infarct region may influence the progression of ischemic stroke by interacting with microglia. Properdin, which is typically secreted by immune cells such as neutrophils, monocytes, and T cells, has been found to possess damage-associated molecular patterns (DAMPs) properties and can perform functions unrelated to the complement pathway. However, the role of properdin in modulating microglia-mediated post-stroke neuroinflammation remains unclear. METHODS: Global and conditional (myeloid-specific) properdin-knockout mice were subjected to transient middle cerebral artery occlusion (tMCAO). Histopathological and behavioral tests were performed to assess ischemic brain injury in mice. Single-cell RNA sequencing and immunofluorescence staining were applied to explore the source and the expression level of properdin. The transcriptomic profile of properdin-activated primary microglia was depicted by transcriptome sequencing. Lentivirus was used for macrophage-inducible C-type lectin (Mincle) silencing in microglia. Conditioned medium from primary microglia was administered to primary cortex neurons to determine the neurotoxicity of microglia. A series of cellular and molecular biological techniques were used to evaluate the proinflammatory response, neuronal death, protein-protein interactions, and related signaling pathways, etc. RESULTS: The level of properdin was significantly increased, and brain-infiltrating neutrophils and macrophages were the main sources of properdin in the ischemic brain. Global and conditional myeloid knockout of properdin attenuated microglial overactivation and inflammatory responses at the acute stage of tMCAO in mice. Accordingly, treatment with recombinant properdin enhanced the production of proinflammatory cytokines and augmented microglia-potentiated neuronal death in primary culture. Mechanistically, recombinant properdin served as a novel ligand that activated Mincle receptors on microglia and downstream pathways to drive primary microglia-induced inflammatory responses. Intriguingly, properdin can directly bind to the microglial Mincle receptor to exert the above effects, while Mincle knockdown limits properdin-mediated microglial inflammation. CONCLUSION: Properdin is a new medium by which infiltrating peripheral myeloid cells communicate with microglia, further activate microglia, and exacerbate brain injury in the ischemic brain, suggesting that targeted disruption of the interaction between properdin and Mincle on microglia or inhibition of their downstream signaling may improve the prognosis of ischemic stroke.

Characteristics and prognostic implications of peripheral blood lymphocyte subsets in patients with anti-MDA5 antibody positive dermatomyositis-interstitial lung disease.

OBJECTIVES: To examine the characteristics of blood lymphocyte subsets in dermatomyositis-interstitial lung disease (DM-ILD) inflicted patients with positive anti-melanoma differentiation-associated gene 5 (anti-MDA5), as well as its prognosis value in this set of patients. METHODS: Data were retrospectively collected from 253 DM-ILD patients from three hospitals in China between January 2016 to January 2021. Patients were grouped into anti-MDA5 antibody positive group (MDA5+ DM-ILD) and anti-MDA5 antibody negative group (MDA5- DM-ILD) based on myositis-specific autoantibody test results. Demographic characteristics, lymphocyte subsets patterns and other clinical features were compared between the two groups. The association of lymphocyte subsets with 180-day mortality was investigated using survival analysis in MDA5+ DM-ILD. RESULTS: Out of 253 eligible patients with DM-ILD, 59 patients were anti-MDA5+ and 194 were anti-MDA5-. Peripheral blood lymphocyte count, CD3+ count, percentage of CD3+, CD3+CD4+ count, and CD3+CD8+ count was lower in MDA5+ DM-ILD than in MDA5- DM-ILD- (all P < 0.001) as well as CD3-CD19+ count (P = 0.04). In MDA5+ DM-ILD, CD3+CD8+ count ≤ 49.22 cell/µL (HR = 3.81, 95%CI [1.20,12.14]) and CD3-CD19+ count ≤ 137.64 cell/µL (HR = 3.43, 95%CI [1.15,10.24]) were independent predictors of mortality. CD3+CD8+ count ≤ 31.38 cell/µL was associated with a higher mortality risk in all DM-ILD patients (HR = 8.6, 95%CI [2.12,31.44]) after adjusting for anti-MDA5 and other clinical characteristics. CONCLUSION: Significant lymphocytes decrease was observed in MDA5+ DM-ILD patients. CD3+CD8+ cell count was associated with worse prognosis in both MDA5+ DM-ILD and all DM-ILD patients.

LncRNA-1810034E14Rik reduces microglia activation in experimental ischemic stroke.

BACKGROUND: Activation of microglial cells plays an important role in neuroinflammation after ischemic stroke. Inhibiting the activation of microglial cells has been suggested as a potential therapeutic approach in the treatment of ischemic stroke. METHODS: Oxygen-glucose deprivation in primary microglial cells and transient middle cerebral artery occlusion (MCAO) in C57BL/6 mice were used as the in vitro and in vivo ischemic stroke models. Microarray analysis was performed to investigate the overall impact of long non-coding RNAs (lncRNAs) on the inflammation status of microglial cells. RT-qPCR was used to evaluate the lncRNA levels and mRNA levels of cytokines and microglial cell markers. ELISA was taken to measure the level of cytokines. Immunofluorescence was used to observe the activation of microglial cells. Western blotting was performed to test the p65 phosphorylation. RESULTS: In this study, we showed that LncRNA-1810034E14Rik was significantly decreased in LPS-treated or oxygen-glucose deprivation-induced microglial cells. Overexpression of 1810034E14Rik decreased the infarct volume and alleviated brain damage in MCAO mice. 1810034E14Rik overexpression reduced the expression of inflammatory cytokines not only in ischemic stroke mice but also in oxygen-glucose deprivation-induced microglial cells. Moreover, 1810034E14Rik overexpression could suppress the activation of microglial cells and inhibit the phosphorylation of p65. CONCLUSIONS: LncRNA-1810034E14Rik plays an anti-inflammatory role in ischemic stroke and regulates p65 phosphorylation, making it a potential target for stroke treatment.

The association between multimorbidity and health-related quality of life: a cross-sectional survey among community middle-aged and elderly residents in southern China.

BACKGROUND: Multimorbidity is common among the middle-aged and elderly residents. And it is associated to the reduction of health-related quality of life (HRQoL), including physical and psychological dimensions. However, there are few studies that have paid attention to the HRQoL of residents with multimorbidity in China. Therefore, this study aims to investigate the relationships between different multimorbidity patterns and HRQoL among middle-aged and elderly adults in China. METHODS: Based on a cross-sectional survey, the information regarding 18,137 adults, who were at least 45 years of age, was collected through interviews. Self-perceived HRQoL was assessed with the EQ-5D-3 L instrument, and the EQ-5D-3 L index score was calculated using the Chinese EQ-5D-3 L value set. The Tobit regression was used to explore the impacts of multimorbidity groups on HRQoL. RESULTS: Of 18,137 respondents, more than a fifth (3773,20.8%) of people had multimorbidity. Mean (SD) of EQ-5D index and VAS values were 0.95(0.14) and 76.02(13.66), respectively. Significant correlations were found between a lower HRQoL and increasing numbers of chronic conditions (P < 0.001). Most of chronic diseases co-occurred frequently, and the association between hypertension and diabetes mellitus was the strongest (adjusted OR = 3.82). The most prevalent disease is hypertension (5052,27.9%), and the most prevalent chronic diseases pair is hypertension and diabetes mellitus (841,4.6%). Among those chronic diseases with high prevalence, the effects on HRQoL ranged from chronic pain to hypertension (adjust b = - 0.036 to - 0.008). In the common multimorbidity patterns, co-occurrence of chronic pain and bone disease (adjust b = - 0.039) had the greatest impact on HRQoL. CONCLUSIONS: The HRQoL of middle-aged and elderly adults declines by multimorbidity. More attention should be paid to the HRQoL of residents with multimorbidity in China. The effect of different multimorbidity patterns on HRQoL is not simply added by two diseases, but changes by the different combination. Identifying different multimorbidity patterns of residents can provide more targeted measures to improve the HRQoL.

A general design strategy for block copolymer directed self-assembly patterning of integrated circuits contact holes using an alphabet approach.

Directed self-assembly (DSA) is a promising lithography candidate for technology nodes beyond 14 nm. Researchers have shown contact hole patterning for random logic circuits using DSA with small physical templates. This paper introduces an alphabet approach that uses a minimal set of small physical templates to pattern all contacts configurations on integrated circuits. We illustrate, through experiments, a general and scalable template design strategy that links the DSA material properties to the technology node requirements.

AZD1390, an ataxia telangiectasia mutated inhibitor, attenuates microglia-mediated neuroinflammation and ischemic brain injury.

AIMS: Excessive neuroinflammation mediated mainly by microglia plays a crucial role in ischemic stroke. AZD1390, an ataxia telangiectasia mutated (ATM) specific inhibitor, has been shown to promote radio-sensitization and survival in central nervous system malignancies, while the role of AZD1390 in ischemic stroke remains unknown. METHODS: Real-time PCR, western blot, immunofluorescence staining, flow cytometry and enzyme-linked immunosorbent assays were used to assess the activation of microglia and the release of inflammatory cytokines. Behavioral tests were performed to measure neurological deficits. 2,3,5-Triphenyltetrazolium chloride staining was conducted to assess the infarct volume. The activation of NF-κB signaling pathway was explored through immunofluorescence staining, western blot, co-immunoprecipitation and proximity ligation assay. RESULTS: The level of pro-inflammation cytokines and activation of NF-κB signaling pathway was suppressed by AZD1390 in vitro and in vivo. The behavior deficits and infarct size were partially restored with AZD1390 treatment in experimental stroke. AZD1390 restrict ubiquitylation and sumoylation of the essential regulatory subunit of NF-κB (NEMO) in an ATM-dependent and ATM-independent way respectively, which reduced the activation of the NF-κB pathway. CONCLUSION: AZD1390 suppressed NF-κB signaling pathway to alleviate ischemic brain injury in experimental stroke, and attenuated microglia activation and neuroinflammation, which indicated that AZD1390 might be an attractive agent for the treatment of ischemic stroke.

QHRD106 ameliorates ischemic stroke injury as a long-acting tissue kallikrein preparation.

Ischemic stroke is the second leading cause of death worldwide, and there are limited effective treatment strategies. QHRD106, a polyethyleneglycol (PEG)-modified long-acting tissue kallikrein preparation, has not been reported previously. In this study, we aimed to investigate the therapeutic effect of QHRD106 in ischemic stroke and its possible mechanism. We found that QHRD106 treatment alleviated brain injury after stroke via bradykinin (BK) receptor B2 (B2R) instead of BK receptor B1 (B1R). Mechanistically, QHRD106 reduced high-mobility group box 1 (HMGB1)-induced apoptosis and inflammation after ischemic stroke in vivo and in vitro. Moreover, we confirmed that QHRD106 reduced the level of acetylated HMGB1 and reduced the binding between heat shock protein 90 alpha family class A member 1 (HSP90AA1) and HMGB1, thus inhibiting the translocation and release of HMGB1. In summary, these findings indicate that QHRD106 treatment has therapeutic potential for cerebral ischemic stroke.

Fraxetin alleviates microglia-mediated neuroinflammation after ischemic stroke.

Background: Neuroinflammation, which is mainly mediated by excessive microglia activation, plays a major role in ischemic stroke. Overactivated microglia secrete numerous inflammatory cytokines, causing excessive inflammatory responses and ultimately exacerbating ischemic brain injury. Hence, compounds that attenuate neuroinflammation could become promising drug candidates for ischemic stroke. Fraxetin has an anti-inflammatory effect in many inflammatory diseases. However, whether it possesses an anti-inflammatory capacity in microglia-mediated neuroinflammation after ischemic brain injury is unknown. Our study aimed to investigate the suppression effect of fraxetin on neuroinflammation in lipopolysaccharide (LPS)-activated microglia and establish whether fraxetin could alleviate ischemic brain injury in a rodent model of ischemic stroke. Methods: For the in vitro experiment, primary microglia were obtained from 1-day-old C57/BL6J mice. The cells were activated with LPS and treated with fraxetin at a non-cytotoxic concentration. Real-time PCR, enzyme-linked immunosorbent assays, and immunofluorescence staining were used to evaluate the anti-inflammatory effects of fraxetin. The potential molecular mechanisms were explored and verified through RNA-sequencing analysis, western blotting and real-time PCR. For the in vivo experiment, focal ischemia was induced by middle cerebral artery occlusion (MCAO) in 8-week-old male C57/BL6J mice. Fraxetin (5 mg/kg) or an equal volume of saline was injected into mice intraperitoneally after MCAO, and 2% 2,3,5-triphenyltetrazolium chloride staining was applied to measure infarct volume. Behavioral tests were conducted to measure neurological deficits in the mice. Real-time PCR, western blotting, and immunofluorescence staining were used to examine the expression of inflammatory cytokines and microglia activation in the ischemic penumbra. Results: Fraxetin effectively inhibited the expression of proinflammatory cytokines including inducible nitric oxide synthase, tumor necrosis factor-α, interleukin-1 beta, and interleukin-6 in LPS-activated microglia. Fraxetin also suppressed the PI3K/Akt/NF-κB signaling pathway in activated microglia, which contributed to its anti-inflammatory effects. Furthermore, the administration of fraxetin attenuated ischemic brain injury and behavioral deficits after stroke. Finally, fraxetin was found to attenuate the activation of microglia both in vitro and in vivo. Conclusions: Our results suggest that fraxetin has a suppression effect on microglia-mediated neuroinflammation, and this effect is associated with the PI3K/Akt/NF-κB signaling pathway. Fraxetin may therefore have potential neuroprotective properties for ischemic stroke.

Imperatorin inhibits mitogen-activated protein kinase and nuclear factor kappa-B signaling pathways and alleviates neuroinflammation in ischemic stroke.

AIMS: Microglia-mediated neuroinflammation plays an important role in the pathological process of ischemic stroke, and the effect of imperatorin on post-stroke neuroinflammation is not fully understood. METHODS: Primary microglia were treated with imperatorin for 2 h followed by LPS (100 ng/ml) for 24 h. The expression of inflammatory cytokines was detected by RT-PCR, ELISA, and Western blot. The activation of MAPK and NF-κB signaling pathways were analyzed by Western blot. The ischemic insult was determined using a transient middle cerebral artery occlusion (tMCAO) model in C57BL/6J mice. Behavior tests were used to assess the neurological deficits of MCAO mice. TTC staining was applied to measure infract volume. RESULTS: Imperatorin suppressed LPS-induced activation of microglia and pro-inflammatory cytokines release and attenuated ischemic injury in MCAO mice. The results of transcriptome sequencing and Western blot revealed that downregulation of MAPK and NF-κB pathways might contribute to the protective effects of imperatorin. CONCLUSIONS: Imperatorin downregulated MAPK and NF-κB signaling pathways and exerted anti-inflammatory effects in ischemic stroke, which indicated that imperatorin might be a potential compound for the treatment of stroke.

γ-Glutamylcysteine Alleviates Ischemic Stroke-Induced Neuronal Apoptosis by Inhibiting ROS-Mediated Endoplasmic Reticulum Stress.

Ischemic stroke is a severe and acute neurological disorder with limited therapeutic strategies currently available. Oxidative stress is one of the critical pathological factors in ischemia/reperfusion injury, and high levels of reactive oxygen species (ROS) may drive neuronal apoptosis. Rescuing neurons in the penumbra is a potential way to recover from ischemic stroke. Endogenous levels of the potent ROS quencher glutathione (GSH) decrease significantly after cerebral ischemia. Here, we aimed to investigate the neuroprotective effects of γ-glutamylcysteine (γ-GC), an immediate precursor of GSH, on neuronal apoptosis and brain injury during ischemic stroke. Middle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation/reoxygenation (OGD/R) were used to mimic cerebral ischemia in mice, neuronal cell lines, and primary neurons. Our data indicated that exogenous γ-GC treatment mitigated oxidative stress, as indicated by upregulated GSH and decreased ROS levels. In addition, γ-GC attenuated ischemia/reperfusion-induced neuronal apoptosis and brain injury in vivo and in vitro. Furthermore, transcriptomics approaches and subsequent validation studies revealed that γ-GC attenuated penumbra neuronal apoptosis by inhibiting the activation of protein kinase R-like endoplasmic reticulum kinase (PERK) and inositol-requiring enzyme 1α (IRE1α) in the endoplasmic reticulum (ER) stress signaling pathway in OGD/R-treated cells and ischemic brain tissues. To the best of our knowledge, this study is the first to report that γ-GC attenuates ischemia-induced neuronal apoptosis by suppressing ROS-mediated ER stress. γ-GC may be a promising therapeutic agent for ischemic stroke.

Nanowire photodetectors.

The use of nanowires and nanowire structures as photodetectors is an emerging research topic. Despite the large amount of reports on nanowire photoresponse that appeared in the literature over the last decade, the mechanism leading to high photosensitivity and photoconductive gain in high aspect ratio nanostructures has been elucidated only recently. Novel device architectures integrated in single nanowire devices are also being actively studied and developed. In this article, the general nanowire photodetector concepts are reviewed, together with a detailed description of the physical phenomena occurring in nanowire photoconductors and phototransistors, with some examples from recent experimental results obtained in our groups. An outlook on future directions toward the use of semiconductor nanowire photoconductors as intrachip interconnects, single-photon detectors, and image sensors, is also given.

Direct heteroepitaxy of vertical InAs nanowires on Si substrates for broad band photovoltaics and photodetection.

Catalyst-free, direct heteroepitaxial growth of vertical InAs nanowires on Si(111) substrates was accomplished over a large area by metal-organic chemical vapor deposition. Nanowires showed very uniform diameters and a zinc blende crystal structure. The heterojunctions formed at the interface between the n-type InAs nanowires and the p-type Si substrate were exploited to fabricate vertical array photodiode devices which showed an excellent rectification ratio and low reverse leakage current. Temperature-dependent current transport across the heterojunctions was studied theoretically and experimentally in the dark and under AM 1.5 illumination. When operated in photovoltaic mode, the open-circuit voltage was found to increase linearly with decreasing temperature while the energy conversion efficiency changed nonmonotonically with a maximum of 2.5% at 110 K. Modeling of the nanowire/substrate heterojunctions showed good agreement with the experimental observations, and allowed determining the conduction band offset between the InAs nanowires and Si to be 0.10-0.15 eV. The external quantum efficiency and photoresponsivity profiles of the device showed a broad spectral response from the visible to the infrared region, indicating potential applications as a broad band photovoltaic cell or a visible-infrared dual-band photodetector.

Poncirin suppresses lipopolysaccharide (LPS)-induced microglial inflammation and ameliorates brain ischemic injury in experimental stroke in mice.

BACKGROUND: Based on accumulating evidence, excessive activation of microglia-mediated inflammatory responses plays an essential role in ischemic stroke. Poncirin (Pon) exerts anti-hyperalgesic, anti-osteoporotic and anti-tumor effects on various diseases. However, the roles of Pon in microglial activation and the underlying mechanism have not been elucidated. This study aimed to explore whether Pon inhibits lipopolysaccharide (LPS)-induced microglial neuroinflammation and protects against brain ischemic injury in experimental stroke in mice. METHODS: Primary microglia cells were prepared from the cerebral cortices of 1- to 2-day-old C57BL/6J mice. Murine BV2 cells and primary microglia were stimulated with LPS and the effects of a non-cytotoxic concentration of Pon on LPS-stimulated pro-inflammatory factors were measured using real-time PCR and enzyme-linked immunosorbent assays (ELISAs). Western blot analyses were used for mechanistic studies. In an in vivo study, 8-week-old male C57BL/6J mice were subjected to focal cerebral ischemia through middle cerebral artery occlusion (MCAO). Pon (30 mg/kg, i.p.) or the same volume of saline was administered after the MCAO model was established, and the infarct volume was evaluated using 2,3,5-triphenyltetrazolium chloride (TTC) staining. We also evaluated animal behaviours, the expression of pro-inflammatory cytokines and microglial activation in the ischemic hemisphere. RESULTS: Pon prevented the release of nitric oxide (NO), prostaglandin E2 (PGE2), interleukin (IL)-1ß, IL-6 and tumor necrosis factor-alpha (TNF-α) in both BV2 cells and primary microglia stimulated with LPS. The inhibitory effects of Pon were associated with the regulation of the ERK1/2, JNK and nuclear factor kappa B (NF-κB) signaling pathways. In mice that underwent MCAO, Pon administration decreased the lesion size and improved neurological deficits. Furthermore, Pon attenuated the production of inflammatory cytokines mainly by restraining microglial activation after ischemic stroke. CONCLUSIONS: Based on the findings from the present study, Pon provides neuroprotection through its anti-inflammatory effects on microglia and it may be a useful treatment for ischemic stroke.

Neuroprotective effects of ZL006 in Aß1-42-treated neuronal cells.

Amyloid beta (Aß)-induced neurotoxicity and oxidative stress plays an important role in the pathogenesis of Alzheimer's disease (AD). ZL006 is shown to reduce over-produced nitric oxide and oxidative stress in ischemic stroke by interrupting the interaction of neuronal nitric oxide synthase and postsynaptic density protein 95. However, few studies are reported on the role of ZL006 in AD. To investigate whether ZL006 exerted neuroprotective effects in AD, we used Aß1-42 to treat primary cortical neurons and N2a neuroblastoma cells as an in vitro model of AD. Cortical neurons were incubated with ZL006 or dimethyl sulfoxide for 2 hours and treated with Aß1-42 or NH3•H2O for another 24 hours. The results of cell counting Kit-8 (CCK-8) assay and calcein-acetoxymethylester/propidium iodide staining showed that ZL006 pretreatment rescued the neuronal death induced by Aß1-42. Fluorescence and western blot assay were used to detect oxidative stress and apoptosis-related proteins in each group of cells. Results showed that ZL006 pretreatment decreased neuronal apoptosis and oxidative stress induced by Aß1-42. The results of CCK8 assay showed that inhibition of Akt or NF-E2-related factor 2 (Nrf2) in cortical neurons abolished the protective effects of ZL006. Moreover, similar results were also observed in N2a neuroblastoma cells. ZL006 inhibited N2a cell death and oxidative stress induced by Aß1-42, while inhibition of Akt or Nrf2 abolished the protective effect of ZL006. These results demonstrated that ZL006 reduced Aß1-42-induced neuronal damage and oxidative stress, and the mechanisms might be associated with the activation of Akt/Nrf2/heme oxygenase-1 signaling pathways.

TMEM16A Inhibition Preserves Blood-Brain Barrier Integrity After Ischemic Stroke.

The inflammatory response plays a pivotal role in Blood-Brain Barrier (BBB) destruction following ischemic brain injury. Enhanced leukocyte adhesion to vascular endothelial cells is an essential event in the inflammatory process. TMEM16A, a newly discovered protein regulating calcium-activated chloride channels, is widely expressed in eukaryotes. Recent studies have suggested that upregulated expression of TMEM16A is associated with the occurrence and development of many diseases. However, the role of TMEM16A in regulating BBB integrity after ischemic stroke has not been fully investigated. In this study, we found that TMEM16A is mainly expressed in brain endothelial cells and upregulated after ischemic stroke in the mouse brain. Caccinh-A01, an TMEM16A inhibitor that reduced its upregulation, attenuated brain infarct size and neurological deficits after ischemic stroke. ICAM-1 and MPO expression and BBB permeability were decreased after TMEM16A inhibitor administration. In addition, TMEM16A silencing rescued oxygen-glucose deprivation/reoxygenation (OGD/R)-induced transendothelial permeability in vitro accompanied by decreased ICAM-1 expression and leukocyte adhesion. Furthermore, our mechanistic study showed that TMEM16A knockdown alleviated NF-κB activation and nuclear translocation, indicating that TMEM16A knockdown downregulated OGD/R-induced ICAM-1 expression in an NF-κB-dependent manner. Finally, NF-κB inhibitor treatment also alleviated OGD/ R-induced BBB permeability, confirming that activated NF-κB and increased ICAM-1 are essential factors involved in ischemia-induced BBB damage. Thus, our research provides a promising treatment strategy against BBB destruction after ischemic stroke, and TMEM16A may become a potential target for the treatment of ischemic stroke.

A systematic study on the growth of gaas nanowires by metal-organic chemical vapor deposition.

The epitaxial growth of GaAs nanowires (NWs) on GaAs(111)B substrates by metal-organic chemical vapor deposition has been systematically investigated as a function of relevant growth parameters, namely, temperature, arsine (AsH3) and trimethyl-gallium (TMGa) flow rates, growth time, and gold nanoparticle catalyst size. When growing in excess As conditions (V/III molar ratios greater than four), the NW growth rate is independent of AsH3 concentration, while it is linearly dependent on TMGa concentration, and it is thermally activated. The NW morphology is primarily affected by the growth temperature, with very uniform NWs growing at around 400 degrees C and severely tapered NWs growing above 500 degrees C. A simple phenomenological expression that allows prediction of the NW growth rate over a wide range of growth parameters has been derived. The growth rate dependence on the seed nanoparticle size has also been investigated, which reveals valuable information on the role of catalyst supersaturation and Ga surface diffusion in the growth mechanism. The NW growth rate is found to be almost independent of Au nanoparticle size down to diameters of approximately 20 nm over a wide range of temperatures and TMGa and AsH3 molar flows. For smaller NW radii, the growth rate becomes size-dependent and is strongly affected by the V/III molar ratio; at relatively low V/III ratios, smaller NWs grow more slowly due to the Gibbs-Thompson effect, while at higher V/III ratios (V/III >50), Ga adatom diffusion becomes the dominant mass-transport mechanism, and smaller NWs grow faster than larger ones. The growth-limiting mechanisms in the above growth regimes are finally discussed, and important quantities such as pyrolysis efficiency of the precursors, supersaturation, and surface diffusion length are deduced by comparing the experimental results with the NW growth rates predicted from first principles.

Heteroepitaxial growth of vertical GaAs nanowires on Si(111) substrates by metal-organic chemical vapor deposition.

Epitaxial growth of vertical GaAs nanowires on Si(111) substrates is demonstrated by metal-organic chemical vapor deposition via a vapor-liquid-solid growth mechanism. Systematic experiments indicate that substrate pretreatment, pregrowth alloying temperature, and growth temperature are all crucial to vertical epitaxial growth. Nanowire growth rate and morphology can be well controlled by the growth temperature, the metal-organic precursor molar fraction, and the molar V/III ratio. The as-grown GaAs nanowires have a predominantly zinc-blende crystal structure along a <111> direction. Crystallographic {111} stacking faults found perpendicular to the growth axis could be almost eliminated via growth at high V/III ratio and low temperature. Single nanowire field effect transistors based on unintentionally doped GaAs nanowires were fabricated and found to display a strong effect of surface states on their transport properties.

Quantum size effects on the perpendicular upper critical field in ultrathin lead films.

We report the thickness-dependent (in terms of atomic layers) oscillation behavior of the perpendicular upper critical field Hc2perpendicular in the ultrathin lead films at the reduced temperature (t = T/Tc). Distinct oscillations of the normal-state resistivity as a function of film thickness have also been observed. Compared with the Tc oscillation, the Hc2perpendicular shows a considerable large oscillation amplitude and a pi phase shift. The oscillatory mean free path caused by the quantum size effect plays a role in Hc2perpendicular oscillation.

Superconductivity modulated by quantum size effects.

We have fabricated ultrathin lead films on silicon substrates with atomic-scale control of the thickness over a macroscopic area. We observed oscillatory behavior of the superconducting transition temperature when the film thickness was increased by one atomic layer at a time. This oscillating behavior was shown to be a manifestation of the Fabry-Perot interference modes of electron de Broglie waves (quantum well states) in the films, which modulate the electron density of states near the Fermi level and the electron-phonon coupling, which are the two factors that control superconductivity transitions. This result suggests the possibility of modifying superconductivity and other physical properties of a thin film by exploiting well-controlled and thickness-dependent quantum size effects.